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Fgf23 and mineral metabolism in the early post-renal transplantation period

Authors :
Wesseling-Perry, Katherine
Pereira, Renata C.
Tsai, Eileen
Ettenger, Robert
Juppner, Harald
Salusky, Isidro B.
Source :
Pediatric Nephrology. November 1, 2013, Vol. 28 Issue 11, p2207, 9 p.
Publication Year :
2013

Abstract

Background The relationship between fibroblast growth factor 23 (FGF23) and vitamin D production and catabolism post-renal transplantation has not been characterized. Methods Circulating creatinine, calcium, phosphorus, albumin, parathyroid hormone, FGF23, and 1,25[(OH).sub.2] vitamin D (calcitriol) values were obtained pre-transplantation, daily postoperatively for 5 days, and at 6 months post-transplantation in 44 patients aged 16.4 ± 0.4 years undergoing renal transplantation at UCLA from 1 August 2005 through to 30 April 2007. 25(OH) Vitamin D and 24,25[(OH).sub.2] vitamin D concentrations were obtained at baseline and on post-operative days 5 and 180, and urinary concentrations of creatinine, phosphorus, and FGF23 were measured on post-operative days 1, 3, 5, and 180. Results Circulating phosphate concentrations declined more rapidly and the fractional excretion of phosphorus was higher in the first week post-transplantation in subjects with higher FGF23 values. Fractional excretion of FGF23 was low at all time-points. Circulating 1,25[(OH).sub.2] vitamin D levels rose more rapidly and were consistently higher in patients with lower FGF23 values; however, 25(OH) vitamin D and 24,25[(OH).sub.2] vitamin D values were unrelated to FGF23 concentrations. Conclusions Inhibition of renal 1α-hydroxylase, rather than stimulation of 24-hydroxylase, may primarily contribute to the relationship between FGF23 values and calcitriol. The rapid decline in FGF23 levels post-transplantation in our patient cohort was not mediated solely by the filtration of intact FGF23 by the new kidney. Keywords FGF23 * PTH Vitamin * D Renal transplantation * Phosphorus<br />Introduction Fibroblast growth factor 23 (FGF23), a phosphaturic hormone that suppresses renal 1 α-hydroxylase activity, has been implicated in the development of secondary hyperpara-thyroidism in chronic kidney disease (CKD) [1], [...]

Details

Language :
English
ISSN :
0931041X
Volume :
28
Issue :
11
Database :
Gale General OneFile
Journal :
Pediatric Nephrology
Publication Type :
Academic Journal
Accession number :
edsgcl.348216565
Full Text :
https://doi.org/10.1007/s00467-013-2547-z